The requirement of bifoveal fixation imposes the need for the visual system to detect and respond to retinal disparity. A failure of this capacity results in strabismus. The features of the neural mechanisms of disparity detection are therefore relevant to our understanding of the etiology of oculomotor imbalance in general an strabismus in particular. Recently, subclinical defects in the sensory and oculomotor responses to retinal disparity have been disclosed in a relatively high percentage (20-30%) of the general population. The evidence suggests that these defects, which are termed stereo-anomaly and vergence-anomaly respectively, are implicated in the etiology of strabismus. Specifically, it has been proposd that strabismus results from the genetic transmission of disparity-anomalies affecting both crossed and uncrossed disparities. Vergence anomalies also are implicated in the etiology of fixation disparity. A model proposed by Ogle some years ago to account for individual differences in fixation disparity-prism curves predicts the presence of such anomalies. The proposed research is designed to test the role of vergence-anomaly in the etiology of strabismus and oculomotor imbalance by examination of the disparity-induced eye movements in normal and strabismus subjects. The mode of inheritane of vergence-anomaly and its possible genetic relationship to strabismus will be evaluated using an objective, computer-controlled testing procedure on several generations of human subjects. Also, other features of disparity-induced eye movements are to be investigated to further our knowledge of the physiological processes of disparity detection.